ERBB2 and neoplasm: Compared with T-DM1, T-DXd adopts a stable hydrophilic linker in systemic circulation, which can precisely control drug release to the tumor site; the toxin of the new mechanism improves drug resistance, and T-DXd has good cell membrane permeability, which can not only kill HER2-positive tumor cells, but also kill adjacent tumor cells through the bystander effect [81].